Elsevier

Atherosclerosis

Volume 164, Issue 2, October 2002, Pages 355-359
Atherosclerosis

C-reactive protein and multiple complex coronary artery plaques in patients with primary unstable angina

https://doi.org/10.1016/S0021-9150(02)00129-6Get rights and content

Abstract

The aim of this study was to investigate the possible association of plasma C-reactive protein (CRP) levels with the presence of angiographically multiple complex lesions (CLs) in patients with primary unstable angina (PUA). For the purpose of this study, 228 consecutive patients with PUA who underwent in-hospital catheterization were evaluated. Plasma CRP levels were measured upon patients’ admission. Coronary plaques were classified as CL or non-CL according to Ambrose's criteria. There were 100 (43.9%) patients with no or one CL (⩽1) and 128 (56.1%) patients with multiple CLs (⩾2). Tertiles of plasma CRP levels upon admission were significantly associated with the number of CLs on angiographic studies. In particular there was a significant gradual increase in either the number of CLs, or the presence of apparently thrombus-containing CLs with increasing of CRP tertiles. By multivariate analysis CRP was independently associated with the presence of either multiple CLs (R.R.=1.8, 95%CI=1.5–2.2, P<0.001), or angiographically apparent thrombus-containing CLs (R.R.=1.4, 95%CI=1.2–1.7, P=0.03).

High plasma levels of CRP may reflect a multifocal activation of the coronary tree in patients with PUA. This finding suggests a generalized inflammatory reaction throughout the coronary tree in these patients.

Introduction

Primary unstable angina (PUA) results mainly from coronary artery thrombosis superimposed on sites of plaque fissure, rupture or superficial erosion [1]. The components of the disrupted plaque, the superimposed thrombosis, and intraplaque bleeding, all contribute to the delineation of the angiographically rough contour of the so called complex lesion (CL) [2], [3], [4], [5].

The disruption of the fibrous cap occurs mainly at the rupture-prone shoulders of the coronary plaque, which are areas of accumulated inflammatory cells [6], [7], [8], [9]. It has been postulated that activation of the plaque-infiltrating inflammatory cells may play an important role in plaques disruption resulting to the induction of acute coronary events.

Although the focus of inflammation of a single plaque is so small that systematic signs of inflammation might not be expected [10], however acute-phase reactants are increased in acute coronary events. In particular, plasma levels of C-reactive protein (CRP) are increased in a significant proportion of patients with unstable coronary artery disease and this increase is significantly associated with either short- or long-term ischemic complications [11].

Moreover, there is an increased body of evidence that supports a multifocal pattern of plaque disruption throughout the coronary artery tree during acute coronary events [12], [13], [14], [15]. It is possible that in some patients, multiple coronary plaques become inflamed, vulnerable and probably ruptured during acute coronary syndromes. Accordingly, the hypothesis that more than one ruptured, thrombotic, and therefore angiographically CLs may be found in patients with PUA and that the number of these CLs may be associated with plasma CRP levels, seems possible. The aim of this prospective study was to evaluate this hypothesis.

Section snippets

Study patients

The study population constituted 271 consecutive eligible patients with PUA who were admitted at our institute. Eligible patients fulfilled the following criteria: (a) new rest angina during the last 12 h lasting ⩾5 but <30 min; (b) diagnostic electrocardiographic ST-segment depression of at least 1, 2 mm after the J point in ⩾2 contiguous leads or T waves inversion >1 mm in leads with predominant R waves. Exclusion criteria were: (a) elevated creatin kinase-MB (⩾17 IU/l, upper normal value) or

Statistical analysis

Continuous variables were expressed as mean±SD for normally distributed and as median with range for non-normally distributed CRP values. Dichotomous variables were presented as percentages. Patients were classified into three groups according to the tertiles of CRP values upon admission. Comparisons of continuous variables among CRP groups were made using ANOVA test, or Kruskal-Wallis test, as appropriate. Bonferroni in ANOVA, t-test, or Mann–Whitney U test were used, as appropriate, for

Results

The mean age of the 228 study patients was 62±9 years (range: 35 through 82 years). There were 168 (73.7%) males. Median CRP value upon admission was 2.35 mg/l (range: 0.12 through 29.9 mg/l). The mean time interval from patients’ symptoms initiation through admission (pre-hospital delay) was 6.3±3.4 h. There was no significant relationship between pre-hospital delay and CRP values upon patients’ admission (r=0.09, P=0.24). Differences among tertiles of CRP regarding to the baseline

Discussion

The primary finding of this study is that in a significant proportion of patients with PUA a multifocal activation of the coronary artery tree is present and the extent of this activation is positively related to plasma CRP levels. The results of the present study suggest a generalized active inflammatory process throughout the coronary tree during acute coronary syndromes. This generalized inflammatory process may induce both a multifocal destabilization of multiple coronary plaques and

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